Targeting macrophage autophagy for inflammation resolution and tissue repair in inflammatory bowel disease

Inflammatory bowel disease (IBD) is a chronic, non-specific, recurrent inflammatory disease, majorly affecting the gastrointestinal tract. Due to its unclear pathogenesis, the current therapeutic strategy for IBD is focused on symptoms alleviation. Autophagy is a lysosome-mediated catabolic process for maintaining cellular homeostasis. Genome-wide association studies and subsequent functional studies have highlighted the critical role of autophagy in IBD via a number of mechanisms, including modulating macrophage function. Macrophages are the gatekeepers of intestinal immune homeostasis, especially involved in regulating inflammation remission and tissue repair. Interestingly, many autophagic proteins and IBD-related genes have been revealed to regulate macrophage function, suggesting that macrophage autophagy is a potentially important process implicated in IBD regulation. Here, we have summarized current understanding of macrophage autophagy function in pathogen and apoptotic cell clearance, inflammation remission and tissue repair regulation in IBD, and discuss how this knowledge can be used as a strategy for IBD treatment.

Automated summary

Inflammatory bowel disease (IBD) is a chronic, non-specific, recurrent inflammatory disease that mainly affects the gastrointestinal tract. Autophagy, a lysosome-mediated catabolic process, has been found to play a critical role in IBD by regulating macrophage function. Macrophages have been shown to be important in maintaining intestinal immune homeostasis and are involved in inflammation remission and tissue repair. This knowledge of macrophage autophagy function in IBD can potentially be used as a strategy for the treatment of IBD.